Tài liệu tiếng anh về hợp chất PCP - PENTACHLOROPHENOL pps

INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
ENVIRONMENTAL HEALTH CRITERIA 71
PENTACHLOROPHENOL
This report contains the collective views of an international group of experts and does not necessarily
represent the decisions or the stated policy of the United Nations Environment Programme, the
International
Labour Organisation, or the World Health Organization.
Published under the joint sponsorship of the United Nations Environment Programme, the International
Labour Organisation, and the World Health Organization
World Health Orgnization
Geneva, 1987
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accidents, coordination of laboratory testing and epidemiological studies, and promotion of research on
the mechanisms of the biological action of chemicals.
ISBN 92 4 154271 3
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CONTENTS
ENVIRONMENTAL HEALTH CRITERIA FOR PENTACHLOROPHENOL
1. SUMMARY
1.1. Identity, physical and chemical properties, analytical methods
1.2. Sources of human and environmental exposure
1.3. Environmental transport, distribution, and transformation
1.4. Environmental levels and human exposure
1.5. Effects on organisms in the environment
1.6. Kinetics and metabolism
1.7. Effects on experimental animals and in vitro test systems
1.8. Effects on man
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS
2.1. Identity
2.1.1. Pentachlorophenol (PCP)
2.1.2. Sodium pentachlorphenate (Na-PCP)
2.1.3. Pentachlorophenyl laurate
2.2. Impurities in pentachlorophenol
2.2.1. Formation of PCDDs and PCDFs during thermal decomposition
2.3. Physical, chemical, and organoleptic properties
2.4. Conversion factors
2.5. Analytical methods
2.5.1. Sampling methods
2.5.2. Analytical methods
3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1. Natural occurrence
3.2. Man-made sources
3.2.1. Industrial production
3.2.1.1 Manufacturing processes
3.2.1.2 Emissions during production
3.2.1.3 Disposal of production wastes
3.2.1.4 Production levels
3.3. Uses
3.3.1. Commercial use
3.3.2. Agricultural use
3.3.3. Domestic use
3.3.4. Use for control of vectors
3.3.5. Formulations
4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION
4.1. Transport and distribution between media
4.1.1. Volatilization
4.1.2. Adsorption
4.1.3. Leaching
4.2. Biotransformation
4.2.1. Abiotic degradation
4.2.2. Microbial degradation
4.2.2.1 Aquatic degradation
4.2.2.2 Degradation in soil
4.3. Degradation by plants
4.4. Ultimate fate following use
4.4.1. General aspects
4.4.2. Disposal of waste water
4.4.3. Incineration of wastes
5. ENVIRONMENTAL LEVELS ANS HUMAN EXPOSURE
5.1. Environmental levels

5.1.1. Air
5.1.2. Water and sediments
5.1.3. Soil
5.1.4. Aquatic and terrestrial organisms
5.1.4.1 Aquatic organisms
5.1.4.2 Terrestrial organisms
5.1.5. Drinking-water and food
5.1.6. Consumer products
5.1.7. Treated wood
5.2. Occupational exposure
5.3. General population exposure
5.4. Human monitoring data
6. KINETICS AND METABOLISM
6.1. Absorption
6.1.1. Animal studies
6.1.2. Human studies
6.2. Distribution
6.2.1. Animal studies
6.2.2. Human studies
6.3. Metabolic transformation
6.3.1. Animal studies
6.3.2. Human studies
6.4. Elimination and excretion
6.4.1. Animal studies
6.4.2. Human studies
6.5. Retention and turnover
6.5.1. Animal studies
6.5.2. Human studies
6.6. Reaction with body components
7. EFFECTS ON ORGANISMS IN THE ENVIRONMENT

7.1. Microorganisms
7.2. Aquatic organisms
7.2.1. Plants
7.2.2. Invertebrates
7.2.3. Vertebrates
7.3. Terrestrial organisms
7.3.1. Plants
7.3.2. Animals
7.4. Population and ecosystem effects
7.5. Biotransformation, bioaccumulation, and
biomagnification
7.5.1. Aquatic organisms
7.5.2. Terrestrial organisms
8. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO TEST SYSTEMS
8.1. Acute toxicity
8.2. Short-term toxicity
8.2.1. Pure or purified PCP
8.2.2. Technical grade PCP
8.2.3. Comparative studies
8.3. Long-term toxicity
8.4. Effects on reproduction and fetal development
8.5. Mutagenicity
8.6. Carcinogenicity
8.7. Other studies
8.8. Contaminants affecting toxicity
8.8.1. Octachlorodibenzodioxin (OCDD)
8.8.2. Heptachlorodibenzodioxin (H7CDD)
8.8.3. Hexachlorodibenzodioxin (H6CDD)
8.8.4. Polychlorinated dibenzofurans (PCDFs)
8.8.5. Polychlorodiphenyl ethers (PCDPEs)

8.8.6. Other microcontaminants
8.9. Mechanism of toxicity
9. EFFECTS ON MAN
9.1. Acute toxicity - poisoning incidents
9.2. Effects of short- and long-term exposures
9.2.1. Occupational exposure
9.2.1.1 Skin and mucous membranes
9.2.1.2 Liver and kidney
9.2.1.3 Blood and haemopoetic system
9.2.1.4 Nervous system
9.2.1.5 Immunological system
9.2.1.6 Reproduction
9.2.1.7 Cytogenetic effects
9.2.1.8 Carcinogenicity
9.2.1.9 Other systems
9.2.2. General population exposure
10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT
10.1. Evaluation of human health risks
10.1.1. Occupational exposure
10.1.1.1 Exposure levels and routes
10.1.1.2 Toxic effects
10.1.1.3 Risk evaluation
10.1.2. Non-occupational exposure
10.1.2.1 Exposure levels and routes
10.1.2.2 Risk evaluation
10.1.3. General population exposure
10.1.3.1 Exposure levels and routes
10.1.3.2 Risk evaluation
10.2. Evaluation of effects on the environment
10.3. Conclusions

11. RECOMMENDATIONS
11.1. Environmental contamination and human exposure
11.2. Future research
11.2.1. Human exposure and effects
11.2.2. Effects on experimental animals and in vitro test systems
11.2.3. Effects on the ecosystem
12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES REFERENCES WHO TASK GROUP ON PENTACHLOROPHENOL
Members
…
NOTE TO READERS OF THE CRITERIA DOCUMENTS
Every effort has been made to present information in the criteria documents as accurately as possible
without unduly delaying their publication. In the interest of all users of the environmental health criteria
documents, readers are kindly requested to communicate any errors that may have occurred to the
Manager of the International Programme on Chemical Safety, World Health Organization, Geneva,
Switzerland, in order that they may be included in corrigenda, which will appear in subsequent volumes.
* * *
A detailed data profile and a legal file can be obtained from the International Register of Potentially
Toxic Chemicals, Palais des Nations, 1211 Geneva 10, Switzerland (Telephone no. 988400 - 985850).
ENVIRONMENTAL HEALTH CRITERIA FOR PENTACHLOROPHENOL
A WHO Task Group on Environmental Health Criteria for Pentachlorophenol met at the Fraunhofer
Institute for Toxicology and Aerosol Research, Hanover, Federal Republic of Germany from 20 to 24
October, 1986. Dr W. Stöber opened the meeting and welcomed the members on behalf of the host
Institute, and Dr U. Schlottmann spoke on behalf of the Federal Government, who sponsored the meeting.
Dr K.W. Jager addressed the meeting on behalf of the three co-operating organizations of the IPCS
(UNEP/ILO/WHO). The Task Group reviewed and revised the draft criteria document and made an
evaluation of the risks for human health and the environment from exposure to pentachlorophenol.
The drafts of this document were prepared by DR G. ROSNER of the Fraunhofer Institute for
Toxicology and Aerosol Research, Hanover, Federal Republic of Germany, and DR A. GILMAN of the
Health Protection Branch, Ottawa, Canada.
The efforts of all who helped in the preparation and finalization of the document are gratefully

acknowledged.
* * *
Partial financial support for the publication of this criteria document was kindly provided by the United
States Department of Health and Human Services, through a contract from the National Institute of
Environmental Health Sciences, Research Triangle Park, North Carolina, USA - a WHO Collaborating
Centre for Environmental Health Effects. The United Kingdom Department of Health and Social Security
generously supported the costs of printing.
1. SUMMARY
1.1. Identity, Physical and Chemical Properties, Analytical Methods
Pure pentachlorophenol (PCP) consists of light tan to white, needlelike crystals and is relatively
volatile. It is soluble in most organic solvents, but practically insoluble in water at the slightly acidic pH
generated by its dissociation (pKa 4.7). However, its salts, such as sodium pentachlorophenate (Na-PCP),
are readily soluble in water. At the approximately neutral pH of most natural waters, PCP is more than
99% ionized.
Apart from other chlorophenols, unpurified technical PCP contains several microcontaminants,
particularly polychlorinated dibenzo- p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs), of
which H6CDD is the most relevant congener toxicologically. 2,3,7,8-T4CDD has only once been
confirmed in commercial PCP samples (0.25 - 1.1 µg/kg). Depending on the thermolytic conditions,
thermal decomposition of PCP or Na-PCP may yield significant amounts of PCDDs and PCDFs. The use
and the uncontrolled incineration of technical grade PCP is one of the most important sources of PCDDs
and PCDFs in the environment.
Most of the analytical methods used today involve acidification of the sample to convert PCP to its
non-ionized form, extraction into an organic solvent, possible cleaning by back-extraction into a basic
solution, and determination by gas chromatography with electron-capture detector (GC-EC) or other
chromatographic methods as ester or ether derivatives (e.g., acetyl-PCP). Depending on sampling
procedures and matrices, detection limits as low as 0.05 µg/m3 in air or 0.01 µg/litre in water can be
achieved.
1.2. Sources of Human and Environmental Exposure
PCP is mainly produced by the stepwise chlorination of phenols in the presence of catalysts. Until
1984, Na-PCP was partly synthesized by means of the alkaline hydrolysis of hexachlorobenzene, but it is

now produced by dissolving PCP flakes in sodium hydroxide solution.
World production of PCP is estimated to be of the order of 30 000 tonnes per year. Because of their
broad pesticidal efficiency spectrum and low cost, PCP and its salts have been used as algicides,
bactericides, fungicides, herbicides, insecticides, and molluscicides with a variety of applications in the
industrial, agricultural, and domestic fields. However, in recent years, most developed countries have
restricted the use of PCP, especially for agricultural and domestic applications.
PCP is mainly used as a wood preservative, particularly on a commercial scale. The domestic use of
PCP is of minor importance in the overall PCP market, but has been of particular concern because of
possible health hazards associated with the indoor application of wood preservatives containing PCP.
1.3. Environmental Transport, Distribution, and Transformation
The relatively high volatility of PCP and the water solubility of its ionized form have led to widespread
contamination of the environment with this compound. Depending on the solvent, temperature, pH, and
type of wood, up to 80% of PCP may evaporate from treated wood within 12 months.
The adsorption and leaching behaviour of PCP varies from soil to soil. Adsorption of PCP decreases
with rising pH and so PCP is most mobile in mineral soils, and least mobile in acidic clay and sandy soils.
Solid or water-dissolved PCP can be photolysed by sunlight within a few days, yielding aromatic
(lower chlorinated phenols, etc.) and nonaromatic fragments, as well as hydrogen chloride (HCl) and
carbon dioxide (CO2). Traces of PCDDs, mainly OCDD are formed photochemically on irradiation of
Na-PCP in aqueous solution.
PCP degrading microorganisms have been isolated from waters and soils. High organic matter and
moisture content, median temperatures, and high pH enhance microbial breakdown in soil (half-life = 7 -
14 days). Low oxygen conditions are generally unfavourable for the biodegradation of PCP, allowing it
to persist in soil (half-life = 10 - 70 days under flooded conditions), water (half-life = 80 - 192 days in
anaerobic water), and sediments (10% decomposition within 5 weeks to almost no degradation). Several
studies have proved that PCP can be degraded by activated sludge. However, in full-scale treatment plants
the treatment efficiency is often reduced.
Numerous metabolites have been identified resulting from the methylation, acetylation, dechlorination,
or hydroxylation of PCP. Of the possible metabolites, at least tetrachlorocatechol seems to be relatively
persistent. However, there is a lack of data concerning the fate of the intermediate products of both the
abiotic and biotic degradation of PCP.

1.4. Environmental Levels and Human Exposure
The ubiquitous occurrence of PCP is indicated by its detection, even in ambient air of mountain rural
areas (0.25 - 0.93 ng/m3). In urban areas, PCP levels of 5.7 - 7.8 ng/m3 have been detected.
While elevated PCP concentrations can be found in groundwater (3 - 23 µg/litre) and surface water
(0.07 - 31.9 µg/litre) within wood-treatment areas, the PCP level of surface waters is usually in the range
of 0.1 - 1.0 µg/litre, with maximum values of up to 11 µg/litre. PCP concentrations in the mg/litre range
can be encountered near industrial discharges.
Sediments of water bodies generally contain much higher levels of PCP than the overlying waters. Soil
samples from PCP or pesticide plants contain around 100 µg PCP/kg (dry weight); heavily contaminated
soil (up to 45.6 mg PCP/kg) can be found in the vicinity of wood-treatment areas.
Residues of PCP in the aquatic invertebrate and vertebrate fauna are in the low µg/kg range (wet
weight). Very high levels (up to 6400 µg/kg) are found in fish from waters that are contaminated with
wood preservatives, while sediment-dwelling organisms, such as clams, show PCP levels of up to 133 000
µg/kg. Fish kills result in PCP residues in fish of between 10 and 30 mg/kg.
After agricultural PCP application, birds can be highly contaminated (47 mg/kg wet weight in liver).
Exposure of farm animals to PCP-treated wood shavings used as litter causes a musty taint of the flesh as
a result of contamination with pentachloroanisole, a metabolite of PCP biodecomposition. PCP levels
ranging from not detectable to 8571 µg/kg have been found in the muscle tissue of wild birds.
The general population is exposed to PCP through the ingestion of drinking-water (0.01 - 0.1 µg/litre)
and food (up to 40 µg/kg in composite food samples). Apart from the daily dietary intake (0.1 - 6
µg/person per day) resulting from direct food contamination with PCP, continuous exposure to
hexachlorobenzene and related compounds in food, which are biotransformed to PCP, may be another
important source.
In addition, because of its widespread use, the general population can be exposed to PCP in treated
items such as textiles, leather, and paper products, and above all, through inhalation of indoor air
contaminated with PCP. Generally, PCP concentrations of up to about 30 µg/m3 can be expected, for up
to the first month, after indoor treatment of large surfaces; considerably higher levels (up to 160 µg/m3)
cannot be excluded under unfavourable conditions. In the long term, values of between 1 and 10 µg/m3
are typical PCP concentrations after extensive treatments, though higher levels, up to 25 µg/m3, have
been found in rooms treated one to several years earlier. For comparison, PCP indoor air levels in

untreated houses are generally below 0.1 µg/m3.
According to the usage pattern, the main sources of occupational exposure to PCP are the treatment of
lumber in sawmills and treatment plants, and exposure to treated wood during carpentry and other wood-
working activities. Most of the reported air concentrations at the work-place are below the TWA MAC
value of 500 µg/m3 that has been established by several countries. Occupational exposure to PCP mainly
occurs via inhalation and dermal exposure.
Since the PCP concentrations in the sources (air, food) do not directly indicate the actual PCP intake by
the different routes, extrapolation from urine residue data has been used to estimate human total body
exposure. Mean or median urine-PCP levels range around 10 µg/litre for the general population without
known exposure, around 40 µg/litre for non-occupationally exposed persons, and around 1000 µg/litre for
occupationally exposed people.
The ranges of urine levels observed in exposed and unexposed persons overlap considerably. This
overlap probably occurs because occupational exposure does not necessarily involve high loading, while
non-occupationally exposed people may, in some instances, be exposed to PCP at levels encountered at he
work-place.
1.5. Effects on Organisms in the Environment
As a result of its biocidal properties, PCP negatively affects non-target organisms in soil and water at
relatively low concentrations. Algae appear to be the most sensitive aquatic organisms; as little as 1
g/litre can cause significant inhibition of the most sensitive algal species. Less sensitive species show
EC50 values of around 1 mg/litre.
Most aquatic invertebrates (annelids, molluscs, crustacea) and vertebrates (fish) are affected by PCP
concentrations below 1 mg/litre in acute toxicity tests. Generally, reproductive and juvenile stages are the
most sensitive, with LC50 values as low as 0.01 mg/litre for fish larvae. Low levels of dissolved oxygen,
low pH, and high temperature increase the toxic effects of PCP. Concentrations causing sublethal effects
on fish are in the low µg/litre range. As PCP contamination in many surface waters is in this range,
population and community effects cannot be ruled out. This is also indicated by the substantial alterations
in the community structure of model ecosystems that are induced by PCP.
PCP is accumulated by aquatic organisms. Fresh-water fish show bioconcentration factors of up to
1000 compared to < 100 in marine fish. The portion of PCP taken up, either through the surrounding
water or along the food chain, is probably species specific. PCP taken up by terrestrial plants remains in

the roots and is partly metabolized.
1.6. Kinetics and Metabolism
PCP is readily absorbed through the intact skin and respiratory and gastrointestinal tracts, and
distributed in the tissues. Highest levels are observed in liver and kidney, and lower levels are found in
body fat, brain, and muscle tissue. There is only a slight tendency to bioaccumulate, and so relatively low
PCP concentrations are found in tissues. In rodent species, detoxication occurs through the oxidative
conversion of PCP to tetrachlorohydroquinone, to a small extent also to trichlorohydroquinone, as well as
through conjugation with glucuronic acid. In rhesus monkeys, no specific metabolites have been
detected. In man, metabolism of PCP to tetrachlorohydroquinone seems to occur only to a small extent.
Rats, mice, and monkeys excrete PCP and their metabolites, either free or conjugated with glucuronic
acid, mainly in urine (rodents, 62 - 83%; monkeys, 45 - 75%) and to a lesser extent with the faeces
(rodents, 4 - 34%; monkeys, 4 - 17%). The pharmacokinetic profile following single doses depends on
the species and possibly on the sex of the test animals. Rats and mice eliminate PCP rapidly, with a half-
life of 6 - 27 h. The kinetics in rats follow a biphasic elimination scheme with a comparatively slow
second elimination phase (half-life, 33 - 374 h), perhaps because extensive enterohepatic circulation
retains PCP in the liver. Retention may also be the result of plasma-protein binding of PCP, which seems
to become stronger at lower PCP concentrations.
In rats, 90% of an applied single oral dose is excreted by day 3 with small amounts still remaining in
the liver (0.3%) and kidney (0.05%) after 9 days. On the other hand, monkeys show a much slower
elimination rate (half-life, 41 - 92 h), apparently because they do not metabolize PCP; even 15 days after
oral application of a single dose (10 mg/kg bodyweight), about 11% of the total dose remained in the
body, particularly in the intestines and liver.
The elimination kinetics of PCP in human beings are a controversial subject. A study on 4 male
volunteers ingesting a single oral dose of water-soluble Na-PCP at 0.1 mg/kg body weight showed a rapid
elimination of PCP both in urine (half-life, 33 h) and plasma (30 h). Within 168 h, 74% of the dose was
excreted in urine as free PCP and 12% as its glucuronide, while about 4% was eliminated in the faeces.
In contrast to this study, the application of oral doses of between 0.016 and 0.31 mg PCP/kg body weight
in 40% ethanol revealed a substantially slower PCP excretion rate, with elimination half-lives of 16 days
(plasma) and 18 - 20 days (urine). These low elimination rates have been ascribed to the high protein
binding tendency of PCP.

Some animal data indicate that there may be long-term accumulation and storage of small amounts of
PCP in human beings. The fact that urine- or blood-PCP levels do not completely disappear in some
occupationally exposed people, even after a long absence of exposure, seems to confirm this, though the
biotransformation of hexachlorobenzene and related compounds provides an alternative explanation of
this phenomenon. However, there is a lack of data concerning the long-term fate of low PCP levels in
animals as well as in man. Furthermore, no data are available on the accumulation and effects of
microcontaminants taken up by people together with PCP.
1.7. Effects on Experimental Animals and In Vitro Test Systems
In the main, mammalian studies have been relatively consistent in their demonstration of the effects of
exposure to PCP. In rats, lethal doses induce an increased respiratory rate, a marked rise in temperature,
tremors, and a loss of righting reflex. Asphyxial spasms and cessation of breathing occur soon before
cardiac arrest, which is in turn followed by a rapid, intense rigor mortis.
PCP is highly toxic, regardless of the route, length, and frequency of exposure. Oral LD50 values for a
variety of species range between 27 and 205 mg/kg body weight according to the different solvent
vehicles and grades of PCP. There is limited evidence that the most dangerous route of exposure to PCP
is through the air.
PCP is also an irritant for exposed epithelial tissue, especially the mucosal tissues of the eyes, nose, and
throat. Other localized acute effects include swelling, skin damage, and hair loss, as well as flushed skin
areas where PCP affects surface blood vessels. Exposure to technical formulations of PCP may produce
chloracne. Comparative studies indicate that this is a response to microcontaminants, principally PCDDs,
present in the commercial product. The parent molecule appears responsible for immediate acute effects,
including irritation and the uncoupling of oxidative phosphorylation with a resultant elevated temperature.
Short- and long-term studies indicate that purified PCP has a fairly limited range of effects in test
organisms, primarily rats. Exposure to fairly high concentrations of PCP may reduce growth rates and
serum-thyroid hormone levels, and increase liver weights and/or the activity of some liver enzymes. In
contrast, technical formulations of PCP usually at much lower concentrations can decrease growth rates,
increase the weights of liver, lungs, kidneys, and adrenals, increase the activity of a number of liver
enzymes, interfere with porphyrin metabolism, alter haematological and biochemical parameters and
interfere with renal function. Apparently microcontaminants are the principal active moities in the
nonacute toxicity of commercial PCP.

PCP is fetotoxic, delaying the development of rat embryos and reducing litter size, neonatal body
weight, neonatal survival, and the growth of weanlings. The no-observed-adverse-effect-level (NOAEL)
for technical PCP is a maternal dose of 5 mg/kg body weight per day during organogenesis. The NOAEL
for purified PCP is lower. In one study, it was reported that purified PCP was slightly more
embryo/fetotoxic than technical PCP, presumably because contaminants induced enzymes that detoxified
the parent compound.
PCP is not considered teratogenic, though, in one instance, birth defects arose as an indirect result of
maternal hyperthermia. The NOAEL in rat reproduction studies is 3 mg/kg body weight per day. This
value is remarkably close to the NOAEL mentioned in the previous paragraph, but there are no
orroborating studies in other mammalian species.
PCP has also proved immunotoxic to mice, rats, chickens, and cattle; at least part of this effect is
caused by the parent molecule.
Neurotoxic effects have also been reported, but the possibility that these are due to microcontaminants
has not been excluded.
PCP is not considered carcinogenic for rats. Mutagenicity studies support this conclusion in as much as
pure PCP has not been found to be highly mutagenic. Its carcinogenicity remains questionable because of
shortcomings in these studies. The presence of at least one carcinogenic microcontaminant (H6CDD)
suggests that the potential for technical PCP to cause cancer in laboratory animals cannot be completely
ruled out.
Note: Since the publication of this monograph in 1987, however, the results of adequate carcinogenicity
studies with commercial-grade pentachlorophenol have been published. The conclusions of these studies
are indicated in the addendum to 8.6 Carcinogenicity.
1.8. Effects on Man
The effects of PCP on man are very similar to those reported in experimental animals. Human data
have been obtained primarily from accidental exposures and from the work-place. Unfortunately, there
are few precise estimates of exposure, hence dose-response relationships are difficult to establish in
human beings.
It is clear that the use of PCP may pose a significant hazard with regard to specific aspects of the health
of workers employed in the production or use of PCP. Chloracne, skin rashes, respiratory diseases,
neurological changes, headaches, nausea, and weakness have been documented in workers at numerous

production and manufacturing sites. Similar symptoms have been reported in some inhabitants of houses
treated internally with PCP. Acute intoxications leading to hyperpyrexia and death have been clearly
associated with exposure to the chlorophenol molecule itself, whereas chloracne appears to be an effect of
the PCDD and PCDF microcontaminants. Changes in industrial practice have resulted in fewer high-
dosage, acute exposures, but deaths due to occupational overexposure to PCP are still being reported.
Studies designed to examine biochemical changes in wood-workers exposed to high levels of PCP for
extended periods have failed to indicate statistically significant effects on major organs, neural tissues,
blood elements, the immune system, or reproductive capacity. However, many of these studies were
based on small sample sizes; hence, analyses of trends indicating effects on liver enzymes, kidney
function, T-cell suppression, nerve conduction velocity, etc., have not been statistically significant.
Others have been non-specific in the search for signs of intoxication in large groups of workers.
However, there are mounting indications that long-term exposure to relatively high levels of PCP leading
to blood-plasma concentrations as high as 4 ppm is likely to cause borderline effects on some
physiological processes. Some of these effects, especially those involving the liver and the immune
system, may be caused, in whole or in part, by the microcontaminants of these chlorophenols, especially
H6CDD.
Several epidemiological studies from Sweden and the USA have indicated that occupational exposure
to mixtures of chlorophenols is associated with increased incidences of soft tissue sarcomas, nasal and
nasopharyngeal cancers, and lymphomas. In contrast, surveys from Finland and New Zealand have not
detected such relationships. The major deficiency in all of these studies appears to be a lack of specific
exposure data.
There are no conclusive reports of increased incidences of cancers in workers exposed specifically to
PCP; however, there have not been any carefully conducted studies of a suitably exposed occupational
group large enough to provide the necessary statistical power to identify an increase in cancer mortality.
Furthermore, there are few occupational groups that have been exposed to a single chemical, such as PCP.
Finally, the various levels of microcontaminants in different formulations make inferences to PCP in
general difficult.
Persons non-occupationally exposed to technical PCP in rooms complained about relatively unspecific
symptoms (headache, fatigue, hair loss, tonsillitis, etc.); a causative connection with PCP could not be
proved or disproved.

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS
Pentachlorophenol (PCP) and its salt, sodium pentachlorophenate (Na-PCP), are the most important
forms of pentachlorophenol in terms of production and use. Other derivatives such as the potassium salt,
K-PCP, and the lauric acid ester, L-PCP are of minor importance. Reflecting this minor role, few data on
the physical and chemical properties of K-PCP and L-PCP are reported in the literature. Hence, this
section primarly concerns PCP and its sodium salt.
2.1. Identity
2.1.1. Pentachlorophenol (PCP)

Molecular formula: C
6
HCl
5
O
CAS chemical name: Pentachlorophenol
Common synonyms: chlorophen; PCP; penchlorol; penta;
pentachlorofenol; pentachlorofenolo;
pentachlorphenol; 2,3,4,5,6-
pentachlorophenol
Common trade names: Acutox; Chem-Penta; Chem-Tol; Cryptogil
ol; Dowicide 7; Dowicide EC-7; Dow
Pentachlorophenol DP-2 Antimicrobial;
Durotox; EP 30; Fungifen; Fungol; Glazd
Penta; Grundier Arbezol; Lauxtol; Lauxtol
A; Liroprem; Moosuran; NCI-C 54933; NCI-C
55378; NCI-C 56655; Pentacon; Penta-Kil;
Pentasol; Penwar; Peratox; Permacide;
Permagard; Permasan; Permatox; Priltox;
Permite; Santophen; Santophen 20;
Sinituho; Term-i-Trol; Thompson's Wood

Fix; Weedone; Witophen P
CAS registry number: 87-86-5
2.1.2. Sodium pentachlorphenate (Na-PCP)

Molecular formula: C
6
Cl
5
ONa
C
6
Cl
5
ONa x H
2
O (as monohydrate)
Common synonyms: penta-ate; pentachlorophenate sodium;
pentachlorophenol, sodium salt;
pentachlorophenoxy sodium; pentaphenate;
phenol, pentachloro-, sodium derivative
monohydrate; sodium PCP; sodium
pentachlorophenate; sodium
pentachlorophenolate; sodium
pentachlorophenoxide
Common trade names: Albapin; Cryptogil Na; Dow Dormant
Fungicide; Dowicide G-St; Dowicide G;
Napclor-G; Santobrite; Weed-beads;
Xylophene Na; Witophen N
CAS registry number: 131-52-2 (Na-PCP);
27735-64-4 (Na-PCP monohydrate)

2.1.3. Pentachlorophenyl laurate
The molecular formula of pentachlorophenyl laurate is C6Cl5OCOR; R is the fatty acid moiety, which
consists of a mixture of fatty acids ranging in carbon chain length from C6 to C20, the predominant fatty
acid being lauric acid (C12) (Cirelli, 1978b).
2.2. Impurities in Pentachlorophenol
Technical PCP has been shown to contain a large number of impurities, depending on the
manufacturing method (section 3.2.1). These consist of other chlorophenols, particularly isomeric
tetrachlorophenols, and several microcontaminants, mainly polychlorodibenzodioxins (PCDDs),
polychlorodibenzofurans (PCDFs), polychlorodiphenyl ethers, polychlorophenoxyphenols, chlorinated
cyclohexenons and cyclohexadienons, hexachlorobenzene, and polychlorinated biphenyls (PCBs). Table
1 presents analyses of PCP formulations taken from several publications. According to Crosby et al.
(1981), the quality of PCP is depends on the source and date of manufacture. Furthermore, analytical
results may be extremely variable, particularly with regard to earlier results, which should be considered
with caution. Jensen & Renberg (1972) detected chlorinated 2-hydroxydiphenyl ethers, which obviously
may transform to dioxins during gas chromatography, thus giving a false indication of a higher level of
PCDDs. Unlike these "predioxins", other isomers are not direct precursors of dioxins, and are labelled
"isopredioxins".
Table 1. Impurities (mg/kg PCP) in different technical PCP products

Component Specification, producer, PCP content (%)
Tech- Tech- Tech- Techni- Techni-
Techni- Technical
f
nical
a
nical
b
nical
b,e
cal

c,g,h
cal
d,i
cal
e

Monsanto Dow Dow Dow Dow Dyn.
Nobel Rhône-Poulenc
(84.6%) (88.4%) (98%) (90.4%) (ns)
j

(87%) (86%)

Phenols
Tetrachloro- 30 000 44 000 2700 10 4000 ns 50
000 70 000
Trichloro- ns < 1000 500 < 1000 ns 20
ns
Higher chlorinated ns 62 000 5000 ns ns ns
70 000
phenoxyphenols
Dibenzo-p-dioxins
Tetrachloro- < 0.1 < 0.05 < 0.05 < 0.05 < 0.2
k
<
0.001 < 0.01
Pentachloro- < 0.1 ns ns ns < 0.2 ns
ns
Hexachloro- 8 4 < 0.5 1 9 3.5
5

Heptachloro- 520 125 < 0.5 6.5 235 130
150
Octachloro- 1380 2500 < 1.0 15 250 600
600
Dibenzofurans
Tetrachloro- < 4 ns ns ns < 0.2 ns
ns
Pentachloro- 40 ns ns ns < 0.2 0.2
ns
Hexachloro- 90 30 < 0.5 3.4 39 10
ns
Heptachloro- 400 80 < 0.5 1.8 280 60
ns
Octachloro- 260 80 < 0.5 < 1.0 230 150
ns
Hexachlorobenzene ns ns ns 400 ns ns
ns


a
From: Goldstein et al. (1977).
b
From: Schwetz et al. (1974).
c
From: Schwetz et al. (1978).
d
From: Buser (1975).
e
From: Umweltbundesamt (1985).
f

From: Anon (1983b).
g
Purified.
h
Dowicide EC-7.
i
Dowicide 7.
j
ns = not specified.
k
< = below detection limit.
In Fig. 1, the structures and numbering system for the
polychlorinated dibenzodioxins (PCDDs) and dibenzofurans (PCDFs)
are illustrated.
Since the toxicity of PCDDs and PCDFs depends not only on the number but also on the position of
chlorine substituents, a precise characterisation of PCP impurities is essential. The presence of highly
toxic 2,3,7,8-tetrachlorodibenzo- p-dioxin (2,3,7,8-T4CDD) has only been confirmed once in commercial
PCP samples. In the course of a collaborative survey, one out of five laboratories detected 2,3,7,8-
T4CDD in technical PCP and Na-PCP samples at concentrations of 250 - 260 and 890 - 1100 ng/kg,
respectively (Umweltbundesamt, 1985). Buser & Bosshardt (1976) found detectable amounts of T4CDD
(0.05 - 0.23 mg/kg) in some samples of different technical PCP products, but on re-analysis were unable
to confirm the compound's identity. In other cases, T4CDD has not been identified at detection limits of
0.2 - 0.001 mg/kg (Table 1).
The higher polychlorinated dibenzodioxins and dibenzofurans are more characteristic of PCP
formulations (Table 1). Hexachlorodibenzo- p-dioxin (H6CDD), which is also considered
highly toxic and carcinogenic (section 8), was found at levels of 0.03 - 35 mg/kg (Firestone et al., 1972),
9 - 27 mg/kg (Johnson et al., 1973), and < 0.03 - 10 mg/kg (Buser & Bosshardt, 1976). According to
Fielder et al. (1982), the 1,2,3,6,7,9-, 1,2,3,6,8,9-, 1,2,3,6,7,8-, and 1,2,3,7,8,9-isomers of H6CDD have
been detected in technical PCP. The 1,2,3,6,7,8and 1,2,3,7,8,9-H6CDDs predominated in commercial
samples of technical PCP (Dowicide 7) and Na-PCP. Octachloro-dibenzo- p-dioxin (OCDD) is present in

relatively high amounts in unpurified technical PCP (Table 1).
Recently, the identification of 2-bromo-3,4,5,6-tetrachlorophenol as a major contaminant in three
commercial PCP samples (ca. 0.1%) has been reported. This manufacturing by-product has probably not
been detected in other analyses because it is not resolved from the PCP peak by traditional
chromatographic methods (Timmons et al., 1984).
2.2.1. Formation of PCDDs and PCDFs during thermal decomposition
The thermal decomposition of PCP or Na-PCP yields significant amounts of PCDDs and PCDFs,
depending on the thermolytic conditions. For pure PCP, dimerization of PCP has been suggested as an
underlying reaction process; in technical PCP, additional reactions, i.e., dechlorination of higher
chlorinated PCDDs and cyclization of predioxins are involved in forming various and different PCDD
isomers (Rappe et al., 1978b).
Pyrolysis of alkali metal salts of PCP at temperatures above 300 °C results in the condensation of two
molecules to produce OCDD. PCP itself forms traces of OCDD only on prolonged heating in bulk and at
temperatures above 200 °C (Sandermann et al., 1957; Langer et al., 1973; Stehl et al., 1973).
Although present in original technical PCP products, a number of PCDDs, other than OCDD, are
generated during thermal decomposition (290 - 310 °C) in the absence of oxygen (Table 2) (Buser, 1982).
Table 2. PCDDs (mg/kg PCP) in the
pyrolysate of technical PCP and Na-PCP
a

PCP Na-PCP

2,3,7,8-T
4
CDD -
b
-
c
1,2,3,7,8,9-H
6

CDD 53 2.1
1,2,3,6,7,8-H
6
CDD 66 0.95
Total H
6
CDD 455 10.5
H
7
CDD 5200 65
OCDD 15 000 200

a
From: Buser (1982).
b
Detection limit (1 mg/kg).
c
Detection limit (0.25 mg/kg).
2.3. Physical, Chemical, and Organoleptic Properties
Pure pentachlorophenol consists of light tan to white, needlelike crystals. It has a pungent odour when
heated (Windholz, 1976). Its vapour pressure suggests that it is relatively volatile, even at ambient
temperatures. Since PCP is practically insoluble in water at the slightly acidic pH generated by its
dissociation, readily water-soluble salts such as Na-PCP are used as substitutes, where appropriate.
Na-PCP is non-volatile; its sharp PCP odour results from slight hydrolysis (Crosby et al., 1981).
Technical PCP consists of brownish flakes or brownish oiled, dustless flakes, coated with a mixture of
benzoin polyisopropyl and pine oil. Technical Na-PCP consists of cream-coloured beads (Anon.,
1983a,b). Technically pure L-PCP consists of a brown oil that is insoluble in water and alcohols, and
soluble in non-polar solvents, oils, fats, waxes, and plasticizers (Cirelli, 1978b).
PCP is non-inflammable and non-corrosive in its unmixed state, whereas a solution in oil causes
deterioration of rubber (Mercier, 1981).

Because of the electron withdrawal by the ring chlorines, PCP behaves as an acid, yielding water-
soluble salts such as sodium pentachlorophenate. Due to nucleophilic reactions of the hydroxyl group,
PCP can form esters with organic and inorganic acids and ethers with alkylating agents, such as methyl
iodide and diazomethane (Crosby et al., 1981). This property has been used for analytical purposes
(section 2.5.2).
PCP may exist in two forms: the anionic phenolate, at neutral to alkaline pH, and the undissociated
phenol at acidic pH. At pH 2.7, PCP is only 1% ionized; at pH 6.7, it is 99% ionized (Crosby et al.,
1981). Other relevant properties of pure PCP and Na-PCP are shown in Table 3.
PCDDs and PCDFs may also be formed during the combustion of materials treated with either purified
or technical PCP. Smoke from birch leaves impregnated with purified Na-PCP and burnt on an open fire
showed considerably increased amounts of PCDDs compared with the original sample (Table 4). The
mass fragmentograms revealed 14 of the 22 possible T4CDD isomers with 1,3,6,8- and 1,3,7,9-T4CDD as
the main and 2,3,7,8- T4CDD as minor isomers. The formation of PCDFs, including small amounts of
2,3,7,8-T4CDF, during either combustion or micropyrolysis (280 °C, 30 min) was only observed in
technical PCP samples; purified Na-PCP was negative in this respect (Rappe et al., 1978b).
Table 3. Physical, chemical, and organoleptic properties of PCP
and Na-PCP

PCP Na-PCP

Boiling point
a
310 °C (decomposition)
Relative molecular mass
b
266.4 288.3
306.3
(monohydrate)
Melting point
a

191 °C
Density (d
4
22
in g/ml)
b
1.987 2
Vapour pressure kPa (mmHg)
at 20 °C
c
2 x 10
-6
(1.5 x 10
-5
)
at 19 °C
d
6.7 x 10
-7
(5 x 10
-6
)
Saturation vapour density 220
(µg/m
3
) (20 °C)
c
Steam volatility
e
0.167

(g/100 g water vapour)
(100 °C)

Table 3 (contd.)

PCP Na-PCP

Solubility in fat 213
(g/kg) (37 °C)
f
n-Octanol/water partition 4.84 (pH 1.2);
coefficient (log P)
g
3.56 (pH 6.5);
3.32 (pH 7.2);
3.86 (pH 13.5)
pKa (25 °C)
e
4.7
Solubility in water:
(g/litre)
e,h,i
0 °C, pH 5 0.005
20 °C, pH 5 0.014
30 °C, pH 5 0.020
20 °C, pH 7 2
20 °C, pH 8 8
20 °C, pH 10 15 > 200
25 °C 330
Solubility in organic

solvents (g/100 g)
(25 °C)
b
:
acetone 50 35
benzene 15 insoluble
ethanol (95%) 120 65
ethylene glycol 11 40
isopropanol 85 25
methanol 180 25
Odour threshold 1.6 (in water)
(mg/litre)
j
:
Olfactory threshold 0.03 (in water)
(mg/litre)
j
:

a
From: IRPTC (1983).
b
From: Cirelli (1978b).
c
From: Zimmerli (1982).
d
From: Dobbs & Grant (1980).
e
From: Crosby et al. (1981).
f

From: Rippen (1984).
g
From: Kaiser & Valdmanis (1982).
h
From: Gunther et al. (1968).
i
From: Bundesamt für Umweltschutz (1982).
j
From: Dietz & Traud (1978a).
Jansson et al. (1978) observed a very wide range of PCDD concentrations in the smoke from burning
wood chips impregnated with a technical PCP formulation (Table 4). The formation of PCDDs was
favoured by temperatures below 500 °C, oxygen deficit, and lower gas-retention time. The results given
in Table 4 are corrected for the very low background values obtained by burning untreated wood chips.
When technical PCP was burnt in a quartz reactor (600 °C, 10 min), Lahaniatis et al. (1985) identified
the following thermolytic products: pentachlorobenzene, hexachlorobenzene, octachlorostyrole,
octachloronaphthaline, decachlorobiphenyl, H6CDF, OCDF, and OCDD. 2,3,7,8-T4CDD was not
detected at a detection limit of 1 mg/kg PCP.
Olie et al. (1983) found only slightly higher levels of PCDDs and PCDFs in the fly ash of burned new
wood treated with PCP compared with painted wood, which was more than 60 years old.
However, because data were missing on PCDD/PCDF levels in the original samples and on the conditions
of burning, meaningful interpretation of these results is not possible.
2.4. Conversion Factors
1 ppm = 10.9 mg PCP/m3 (25 °C, 101.3 kPa)
1 mg PCP/m3 = 0.09 ppm
Table 4. Amount of PCDDs in the original sample and in
the smoke from combusted materials treated with purified
Na-PCP or technical PCP

Birch leaves
a

Wood chips
b
(mg PCDDs/kg Na-PCP (mg PCDDs/kg PCP
(purified)) (technical))
Original Smoke
c
Original Smoke
c,d
sample sample

T
4
CDD < 0.02 5.2 nd
e
< 4.7 - 47
P
5
CDD < 0.03 14 nd < 1.2 - 419
H
6
CDD < 0.03 56 7 < 9.3 - 93
H
7
CDD 0.3 172 93 < 4.7 - 279
OCDD 0.9 710 186 < 0.9 - 442

a
Adapted from: Rappe et al. (1978b).
b
Adapted from: Jansson et al. (1978).

c
Smoke trapped on charcoal filter.
d
Depending on combustion conditions.
e
nd = not determined.
2.5. Analytical Methods
A number of methods have been used to determine PCP in a variety of media. The earlier procedures
were reviewed by Bevenue & Beckman (1967). They were mostly based on colour reactions, which are
not very specific and relatively insensitive. For several years, more sophisticated devices have been
available to analysts, of which gas chromatography has become the method of choice (Table 5).
Table 5. Analytical methods for the determination of PCP


Medium Sampling method Analytical method Detec-
Detection Reco- Reference
tion limit
very


Air
Air- Impinger collection Derivatization with diazo- EC
a
0.22
mg/m
3
ns
c
Hoben et al.
aerosol with KOH; hexane methane; purification in

(1976a)
extraction chromatoflex Florisil
column; GC
d
analysis
Air Filter and bubbler HPLC
e
analysis; column: UV
254
b
0.27
mg/m
3
95.3- NIOSH
collection; ethylene µ Bondapack C
18
; mobile
100.9% (1978)
glycol extraction phase: methanol/water
Air Bubbler collection; Derivatization with acetyl EC 0.05
µg/m
3
ns Dahms &
absorption in K
2
CO
3
chloride; GC analysis
Metzner
solution; hexane

(1979)
extraction
Air Adsorption on to GC analysis EC 0.5
µg/m
3
ns Zimmerli &
filter papers
Zimmermann
impregnated with
(1979)
adsorbant extraction
concentration in ether
Air Impinger collection; HPLC analysis; column: UV
225
0.5
µg/m
3
ns Woiwode et
absorption in K
2
CO
3
- Lichrosorb C
18
; mobile
al. (1980)
solution; benzene phase: methanol
extraction
Air Air from wood samples GC analysis EC ns
89.7- Warren et

in reactor tube ads- (< 1.5
99.9% al. (1982)
orbed on silica gel; µg/m
3
)
desorption with benzene
Air Impinger collection; Derivatization with acetic EC ns
ns Kauppinen &
absorption in anhydride in presence of
Lindroos
toluene pyridine; GC analysis
(1985)


Table 5. (contd.)


Medium Sampling method Analytical method Detec-
Detection Reco- Reference
tion limit
very


Biological tissues and fluids
Blood Benzene extraction Derivatization with diazo- EC 20
µg/litre 87- Bevenue et
(human) from acidified methane; GC analysis
100% al. (1968)
solution
Blood, Ethyl ether extrac- No derivatization; GC anal- EC-

3
H 0.1 ng
90- Barthel et
urine, tion from acidified ysis; column: 3% diethylene EC-
63
Ni 0.02
ng 100% al. (1969)
tissue solution; NaOH ex- glycol succinate + 2% H
3
PO
4
;
(human) traction; benzene confirmation by MS and TLC
extraction
Organic Hexane/isopropanol Der. with acetic anhydride EC ns
81-91% Rudling
tissues extraction from in presence of pyridine;
(1970)
acidified sample; GC analysis
borax extraction
Urine Ethyl ether extrac- Derivatization with diazo- EC 10
µg/litre 92- Shafik et
(rat) tion from acidified ethane; GC analysis
98% al. (1973)
solution
Adipose NaOH extraction; Derivatization with diazo- EC 5 µg/kg
75% Shafik
tissue diethyl ether methane; GC analysis
(1973)
(human) extraction from

acidified solution
Urine, Acidic hydrolysis No derivatization; negative MS
f
1 ng
90% Dougherty &
seminal (urine); hexane/2- chemical ionization (NCI)
Piotrowska
fluid propanol or hexane/ mass spectrometry; internal
(1976a;b)
(human) ether extraction from standard: p-chlorobenzophenone
acidified solution
Tissue, Hexane or benzene Derivatization with diazo- EC 20
µg/kg 91.4- Hoben et al.
plasma, extraction ethane (urine) or diazo-
95.3% (1976a)
urine methane; purification in
(rat) chromatoflex Florisil column;
GC analysis


Table 5. (contd.)


Medium Sampling method Analytical method Detec-
Detection Reco- Reference
tion limit
very


Tissues Acetone extraction (a) TLC

g
analysis on silica Radio- ns
ns Glickman et
(fish) gel UV
254
; mobile phase: active
al. (1977)
methylene chloride
Acetone extraction (b) Derivatization with MS ns
ns Glickman et
methyl iodide and K
2
CO
3
;
al. (1977)
GC analysis
Urine Hexane extraction Derivatization with acetyl EC 10
µg/litre ns Dahms &
(human) from acidified chloride in the presence of
Metzner
solution pyridine; GC analysis
(1979)
Urine Benzene extraction Derivatization with diazo- EC 1
µg/litre 93.2- Edgerton
(human, from acidified methane; separation of
97.2% et al.
rat) solution methylated phenols in acid
(1979)
alumina column; GC analysis;

GC-MS confirmation
Plasma Benzene extraction Derivatization with acetic EC 50
µg/litre 91- Eben et
(human) anhydride; GC analysis
102% al. (1981)
Urine Acidic or enzymatic Derivatization with acetic EC 20
µg/litre 77- Eben et
(human) hydrolysis; ethyl anhydride; GC analysis
98% al. (1981)
ether extraction;
benzene extraction
Tissues, Diethyl ether (ethyl Purification on Hypersil- UV
216
1 µg/kg
62- Mundy &
serum, acetate-hexane) cartridge; mobile phase:
108% Machin
egg extraction from NaOH methanol; HPLC analysis
(1981)
yolk/ (hydrochloric acid)
white solution; concentra-
tion by evaporation